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  • Title: Effect of angiotensin AT2 and muscarinic receptor blockade on osmotically induced vasopressin release.
    Author: Höhle S, Culman J, Boser M, Qadri F, Unger T.
    Journal: Eur J Pharmacol; 1996 Apr 04; 300(1-2):119-23. PubMed ID: 8741176.
    Abstract:
    Recently, we have shown that angiotensin II-induced AT1 receptor-mediated vasopressin release can be potentiated by blockade of periventricular AT2 receptors. In the present study, we investigated whether the AT2 receptor also exerts an inhibitory effect on osmotically induced vasopressin release. In addition, we tested the effect of the muscarinic receptor antagonist, atropine, on hyperosmolar saline-induced vasopressin release. Plasma vasopressin levels were determined 90 s after intracerebroventricularly applied hyperosmolar saline (0.2, 0.3 and 0.6 M, 5 microliters) with or without intracerebroventricular pretreatment with 1 nmol of the selective AT2 receptor antagonist, PD 123177 (1-(4-amino-3-methylphenyl)methyl-5-diphenylacetyl-4,5,6,7-tetrahy dro- 1H-imidazo[4,5-c]pyridine-6-carboxylic acid-2HCl), or with 15 nmol of the muscarinic receptor antagonist, atropine. PD 123177 potentiated 0.2 M saline-induced vasopressin release (4.7 +/- 0.8 pg/ml vs. 2.2 +/- 0.3 in vehicle-pretreated controls, P < 0.05), did not affect 0.3 M saline-induced vasopressin release (4.3 +/- 0.7 pg/ml vs. 5.4 +/- 0.6 pg/ml in vehicle-pretreated controls) and reduced 0.6 M saline-induced vasopressin release (10.0 +/- 2.3 pg/ml vs. 17.9 +/- 1.8 pg/ml in vehicle-pretreated controls, P < 0.05). Pretreatment with atropine reduced 0.3 M (2.3 +/- 0.6 pg/ml vs. 5.4 +/- 0.9 pg/ml in vehicle-pretreated controls, P < 0.05) and 0.6 M saline-induced AVP release (4.0 +/- 1.5 pg/ml vs. 18.4 +/- 2.4 pg/ml in vehicle-pretreated controls, P < 0.05) but did not affect 0.2 M saline-induced vasopressin release (2.1 +/- 0.4 pg/ml vs. 3.2 +/- 0.8 pg/ml in vehicle-pretreated controls). Our results suggest that the low saline concentration-induced, AT1 receptor-mediated, vasopressin release is under inhibitory control by periventricular AT2 receptors. Following high saline concentrations, a muscarinic mechanism seems to be predominant on which AT2 receptor stimulation acts in a facilitating manner.
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